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[Lactic acidosis in a child with acute severe asthma]
1Service de réanimation pédiatrique, CHU Estaing, 1, place Raymond et Lucie Aubrac, 63003 Clermont-Ferrand, France.
Insights
Lactic acidosis is rare in children with acute severe asthma (ASA). This case report details a pediatric patient who recovered spontaneously from lactic acidosis during ASA treatment.
Area of Science:
- Pediatric Intensive Care Medicine
- Respiratory Medicine
- Emergency Medicine
Background:
- Lactic acidosis is a known complication in adults with acute severe asthma (ASA).
- Pediatric cases of lactic acidosis associated with ASA are infrequently reported.
- Early recognition and management are crucial for pediatric patients with ASA.
Observation:
- A 2-year-old girl presented with ASA requiring high-flow oxygen, intravenous methylprednisolone, and salbutamol.
- During treatment, she developed metabolic acidosis, hypocapnia, elevated anion gap, and high lactate levels.
- Congenital metabolic disease work-up yielded normal results.
Findings:
- The patient exhibited significant lactic acidosis (lactates 8 mmol/L) and metabolic acidosis (pH 7.29, bicarbonate 12 mmol/L, anion gap 20 mmol/L).
- The lactic acidosis resolved spontaneously within 72 hours of intensive care.
- The multifactorial origin of lactic acidosis in ASA was suggested.
Implications:
- Lactic acidosis in pediatric ASA, though rare, requires clinical awareness.
- Prompt identification can prevent potential worsening of respiratory status and unnecessary treatment escalation.
- This case highlights the importance of monitoring metabolic parameters in critically ill children with severe asthma.
Abstract:
Lactic acidosis is a recognized event in adult patients with acute severe asthma (ASA). Only a few cases have been reported in children. Hereinafter is reported the case of a 2-year-old girl hospitalized in the pediatric intensive care unit for ASA, which was treated with high-flow oxygen therapy and intravenous methylprednisolone and salbutamol. During hospitalization, she had metabolic acidosis with a 7.29 pH, a 26mmHg hypocapnia, and a decrease in bicarbonates to 12 mmol/L. The anion gap was increased to 20 mmol/L and lactates to 8 mmol/L. The work-up for a congenital metabolic disease was normal. Progression was propitious with spontaneous improvement of lactic acidosis, and the child was discharged from the intensive care unit after 72 h. The origin of lactic acidosis during ASA seems to be multifactorial. Although its recovery can be spontaneous, it is important to know how to identify it because it can worsen respiratory symptoms and can lead to incongruous therapeutic escalation.
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